Overexpression of MALAT1 contributes to cervical cancer progression by acting as a sponge of miR‐429

Abstract

Cervical cancer remains a malignant type of tumor and is the fourth leading cause of cancer‐related death among females. MALAT1 has been identified as a tumor oncogene in various cancers. Our present study aimed to explore the biological role of MALAT1 in cervical cancer. We observed that MALAT1 was significantly upregulated in human cervical cancer cell lines compared with the ectocervical epithelial cells. MALAT1 was repressed by transfection with LV‐shMALAT1, whereas increased by LV‐MALAT1 in HeLa and Caski cells. Silencing of MALAT1 obviously reduced cervical cell viability, induced cell apoptosis, and repressed cell invasion capacity. Conversely, overexpression of MALAT1 exhibited an opposite phenomenon. Furthermore, miR‐429 was predicted as a direct target of MALAT1, and it was dramatically decreased in cervical cancer cells. It has been shown that miR‐429 plays a crucial role in cervical cancer progression. In our current study, the targeting correlation between MALAT1 and miR‐429 was confirmed by luciferase reporter assays and RIP experiments. Finally, in vivo animal models were established, and we indicated that MALAT1 inhibited cervical cancer progression via targeting miR‐429. These findings revealed that MALAT1 can sponge miR‐429 and regulate cervical cancer pathogenesis in vivo and in vitro. In conclusion, we indicated that the MALAT1/miR‐429 axis was involved in cervical cancer development.

Dihydromyricetin induced lncRNA MALAT1-TFEB-dependent autophagic cell death in cutaneous squamous cell carcinoma

“…The MALAT1 sequences were designed and the objective products were subcloned into pcDNA 3.1 GenePharma (Shanghai, China). The constructed vectors and the lentivirus packaging vectors (pMD2.G) were recotransfected into the cells 16.…”

miR-429 as biomarker for diagnosis, treatment and prognosis of cancers and its potential action mechanisms: A systematic literature review

“…miR-429 was downregulated in CC tissues and CC cells C33A, HeLa, CaSki, SiHa compared with normal tissues and noncancerous ectocervical epithelial cell Ect1/E6E7. Meanwhile, miR-429 overexpression suppressed proliferation and promoted apoptosis of CC cells [34,35]. IKKβ was a target gene of miR-429 and ectopic expression of IKKβ abrogated the phenotypes induced by miR-429.…”

miR‑429 inhibits osteosarcoma progression by targeting HOXA9 through suppressing Wnt/β‑catenin signaling pathway

“…For example, miR-429 expression was downregulated in human thyroid cancer and it inhibited cell growth and promoted cell apoptosis (33). Moreover, miR-429 served as a suppressor in cervical cancer (34) and in pancreatic cancer (35). However, studies concerning miR-429 expression and its functional effect in OS are still rare and it is therefore necessary to investigate the underlying mechanisms of miR-429 in OS.…”